After the
CA the Bordeaux people said I had a 50-50 chance of having a flutter
problem because they were not able to complete the L-Inferior-PV-to-mitral-valve-ring
line. (I do not know the time frame for this prediction; that is, would
the chances be better the longer I went without a breakthrough?)

Since that
time, I have had a number of breakthroughs, which are summarized in the
following table:

Notes: At
each breakthrough, I also took additional Mg, K and taurine.

When trying
to chemically convert, I did not make sure that the AR dose would have
maximum affect by being quickly absorbed and hitting all at once. This I
should have done by crumbling it up and taking it on an empty stomach.
This was especially true for the Dec 7 event, when I ate right after
taking the medications.

It is not
completely clear what triggered the breakthroughs, except that there
seems to be a connection with exercise (as there was early in my AF
career), with running being the most likely culprit; however, I do other
exercise which seems about equal in terms of intensity, duration and HR.
The breakthroughs occur after rather than during exercise, suggesting a
significant vagal component (however, although my HR tends to be low,
but my BP is normal with treatment).

In
consultation with my cardiologist, I have developed the following plan:

1) Stop
running for the time being. (My cardiologist, who is an enthusiastic
exerciser himself, does not think I should necessarily settle for this.)

2) Continue
to exercise at the level I am now, which is 75% weights and provides a
decent workout, but does not push my heart rate much above 100+ or so
for very long (with the beta blocker)*.

3)
Experiment with pushing the limits a bit. About an hour before doing so,
I can take an extra 12.5 mgs metoprolol. I could also take extra
supplemental antioxidants/anti-inflammatories, as well as extra Mg, K
and taurine.

4) If #3
seemed to be working, I could consider going off metoprolol bid (he says
I wouldn’t need to taper off, but I would, just to be that much safer)
and just take it to cover more vigorous exercise. I am tolerating the
dose fairly well, but a couple of times I felt better and realized that
I had missed a dose. Also, my pre-beta blocker resting heart rate, like
most endurance people, was low (50 or so), and now can be lower.

5) If I
went into AF/AFL as the result of the increase and had to be CVed, I
would either drop the more intense exercise and/or start taking
flecainide 50 mgs bid. (Previous to my CA, this dose held me for several
months and might be more effective now because of the work that has been
done.)

6) If the
50 mgs didn’t hold me and I needed to be CVed again, I would go onto
flecainide 100 bid and start planning for a CA.

I very much
appreciate the fact that my cardiologist is very sympathetic to my
desire to maintain an exercise program that meets my needs for living
fully, and that he doesn’t think much of my having to go back on
flecainide; if I had to go to step #6, he’d support having another
ablation.

If I were
to opt for another CA, my choices would be:

1) Return
to the Bordeaux group, who has focused on Continuous AF and has the best
record; however, I would have to pay out of pocket and possibly have a
long wait; however they might be able to slip me in if they believed
that the CA this time would be short;

2) Dr
Natale, who quotes a lower rate of success for Continuous AF; however,
these rates *might* not apply to my case (I would of course ask him
about this, during any consultation). He also does a stepwise procedure
for Continuous AFers as do Drs Jais and Haissaguerre in Bordeaux and Dr
Reddy (see the following);

I had a
breakthrough on March 17 that was to be CVed. During the procedure, my
heart arrested for a couple of minutes before responding to pacing and I
was in junctional rhythm, so a pacemaker was put in (St Jude Zephyr
#5826).

This has resulted in improvement. I no longer have the unpleasant slow
heart rate (low 40's and possibly lower when I am sleeping) and the
accompanying ectopics that may have contributed or at least heralded AF
episodes. And, without the pacemaker, a CV would be too dangerous. With
it, I can be CVed, if necessary.

I am on a small dose of flecainide (12.5 mg x 2) + 180 diltiazem. In
June 2009, pacemaker interrogation revealed that I have been in NSR
since the implacement, with only one tachycardia run of 9 seconds
(according to the pacemaker readout). My atria are being paced most of
the time -- my ventricles not at all, so my AV node is doing its job.
For the time-being, I am satisfied.

For several months, I had been
sensing heart instability (including PVCs), plus I had several short
runs of tachycardia. I hasten to add that these were minimal in number
by any standards, and that it was just that I had become hypervigilant
that they did represent a change that they were upsetting to me.

Then, on July 15, the day
after previous day during which I indulged in some heavy yard work and
exercise (I was beat!), arrhythmia struck shortly after I got up.

It feel like one of those runs
of tachycardia except that it didn't stop. I was less symptomatic than
other episodes. I used PIP to no effect at least at the time: metoprolol
50 mg followed 45 minutes later by 150 flecainide (I forgot to crush it
encourage quick absorption, but I did refrain from eating). This I
repeated 2 hours later.

My cardiologist's office said
(with apologies because they had a full day) that I would have to go
through the ER; they would be called if necessary.

The ER used the same strategy as previously: a
drip of something this time a Ca channel blocker supposed to slow the
heart rate. If I had been a normal patient and this strategy were
successful, this probably would have constituted treatment, even if my
AR remained. My cardiologist, whom I respect and like a lot, but who is
not an EP, knows that I insist on taking steps to getting into NSR and
staying there (see
Choosing treatment for atrial fibrillation.htm#SOME_ASSUMPTIONS).

So, he arranged for me to be admitted to the
hospital to cover the possibility of the increased flecainide dosage
being proarrhythmic. I gently pointed out (to the hospitalist) that I
had been on the increased dose for some time in the past before my
ablations and that I had taken a total of 300 mgs the day before, both
with no ill effects, but (although he understood where I was coming
from) said that this was the rule. A CV was scheduled for the next day.

In any case, I converted at about 1:30 am early
the next morning.

After great discussion and consultation with the
St Jude pacemaker rep (an extraordinarily knowledgeable lady), it was
decided that my AR was indeed flutter, although it was obscured by the
pacemaker responses, both pacing and possibly be one of its sensing
parameters being set incorrectly.

My first question would of course be "Why did
the flutter recur?" There can be no certain answer, but these factors
may have been involved: 1) The break in the LPV-to-mitral valve line
attempted by Dr Jais that the Bordeaux people told me left me with a 50%
chance of flutter; 2) the breakdown of the scarring produced by Wolf MM
(2006) and CA (2007); 3) the development of new foci; 4) the creating of
new AR substrate caused by aging or by my continuing to exercise, even
at a reduced rate; 5) the trigger of the high level of tiring,
dehydrating activity on the previous hot day.

Why did I self-convert? I would assume the
medication (PIP plus increased flecainide dosage and the addition of the
beta blocker) would have helped. Being forced to rest and re-hydrate in
the hospital might have played a role?

What do I do now? I will hope that the increase
in flecainide and the addition of metroprolol will help prevent
further recurrences. I also suggested that my pacemaker minimum
set-point be raised from 50 to 55, as I have sensed that what ectopics I
had occurred when my heart rate was down -- so this might help. Also, I
need to rest more, pay more attention to hydration and realize that any
heavy activity could be a trigger, even if I allow myself to recover.

I probably need to face the fact that the days
of exhilarating, exhausting activity are over.